Involvement of the amygdala in memory storage: Interaction with other brain systems

Abstract

There is extensive evidence that the amygdala is involved in affectively inf luenced memory. The central hypothesis guiding the research reviewed in this paper is that emotional arousal activates the amygdala and that such activation results in the modulation of memory storage occurring in other brain regions. Several lines of evidence support this view. First, the effects of stress-related hormones (epinephrine and glucocorticoids) are mediated by inf luences involving the amygdala. In rats, lesions of the amygdala and the stria terminalis block the effects of posttraining administration of epinephrine and glucocorticoids on memory. Furthermore, memory is enhanced by posttraining intraamygdala infusions of drugs that activate ␤-adrenergic and glucocorticoid receptors. Additionally, infusion of ␤-adrenergic blockers into the amygdala blocks the memory-modulating effects of epinephrine and glucocorticoids, as well as those of drugs affecting opiate and GABAergic systems. Second, an intact amygdala is not required for expression of retention. Inactivation of the amygdala prior to retention testing (by posttraining lesions or drug infusions) does not block retention performance. Third, findings of studies using human subjects are consistent with those of animal experiments. ␤-Blockers and amygdala lesions attenuate the effects of emotional arousal on memory. Additionally, 3-week recall of emotional material is highly correlated with positronemission tomography activation (cerebral glucose metabolism) of the right amygdala during encoding. These findings provide strong evidence supporting the hypothesis that the amygdala is involved in modulating long-term memory storage.For decades there has been controversy over the question of whether the amygdala is involved in memory (1-4). Extensive evidence from many laboratories has now resolved this general controversy. Studies of the effects of lesions of the amygdala in animals and humans leave little doubt that the amygdala is involved in mediating affectively influenced memory (5-8). However, there remains considerable controversy concerning the specific role (or roles) of the amygdala in affectively influenced memory. The findings of lesion studies suggest that the amygdala may enable the formation of stimulus-reward associations (1, 9-11) and may be a site of neuroplasticity mediating aversive learning (12-15). Research from our laboratory using a variety of experimental methods provides extensive additional evidence that the amygdala is involved in memory. However, our findings suggest a somewhat different view of the role of the amygdala in affectively influenced memory. Our findings suggest that the amygdala regulates the storage or consolidation of information in other brain regions (16). The central hypothesis guiding our research is that emotional arousal activates the amygdala and that such activation results in modulation of memory storage processes occurring in brain regions influenced by the amygdala. According to this view, the amygdala is part of a...

Hippocampal neuroplasticity induced by early-life stress: Functional and molecular aspects

“…example, facilitation of memory consolidation [102,117]. From amygdala outflow nuclei [112], selected stress signals project to the hippocampus (via mono-and poly-synaptic projections), evoking IEG expression [55] and enhancing synaptic efficacy [146,20].…”

Overexpression of Proenkephalin in the Amygdala Potentiates the Anxiolytic Effects of Benzodiazepines

“…The amygdala also has high levels of endogenous opioid peptides and opioid receptors (Loughlin et al 1995), and opioid mechanisms have been implicated in many biological functions, including nociception, memory, and fear conditioning (Good and Westbrook 1995;McGaugh et al 1996;Valverde et al 1996). A partial anxiolytic action has been reported following microinjection of morphine into amygdala (File and Rodgers 1979).…”

“…Local infusion of benzodiazepine agonists into the amygdala produces anxiolytic effects which can be blocked by co-administration of GABA A or benzodiazepine antagonists (Scheel-Kruger and Petersen 1982;Petersen et al 1985; Treit 1994, 1995). Furthermore, the anxietyreducing actions of systemic benzodiazepines can be blocked by intra-amygdala injection of GABA/benzodiazepine antagonists (Sanders and Shekhar 1995).The amygdala also has high levels of endogenous opioid peptides and opioid receptors (Loughlin et al 1995), and opioid mechanisms have been implicated in many biological functions, including nociception, memory, and fear conditioning (Good and Westbrook 1995;McGaugh et al 1996;Valverde et al 1996). A partial anxiolytic action has been reported following microinjection of morphine into amygdala (File and Rodgers 1979).…”

Modulation of long-term memory by arousal in alexithymia: The role of interpretation

“…A variety of substances, including glucose and the adrenal hormones epinephrine and norepinephrine, are released into the bloodstream during times of arousal, stress and emotion, which indirectly alter brain stem and amygdalar function (Gold, 2005;Hamann, 2001;McGaugh, 2000;McGaugh, Cahill, & Roozendaal, 1996). When administered soon after learning, these substances alter memory in a classic ''inverted-U'' manner, whereby moderate amounts enhance performance and low or high amounts can impair or fail to influence performance (McGaugh, 2000;Yerkes & Dodson, 1908).…”